Abstract

Chronic obstructive pulmonary disease (COPD) and idiopathic pulmonary fibrosis are regarded as a diseases of accelerated lung ageing and show all of the hallmarks of ageing, including telomere shortening, cellular senescence, activation of PI3 kinase-mTOR signaling, impaired autophagy, mitochondrial dysfunction, stem cell exhaustion, epigenetic changes, abnormal microRNA profiles, immunosenescence and a low grade chronic inflammation due to senescence-associated secretory phenotype (SASP). Many of these ageing mechanisms are driven by exogenous and endogenous oxidative stress. There is also a reduction in anti-ageing molecules, such as sirtuins and Klotho, which further accelerate the ageing process. Understanding these molecular mechanisms has identified several novel therapeutic targets and several drugs and dietary interventions are now in development to treat chronic lung disease.

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